Cancer remains a major health problem worldwide and ranks as the second most common cause of death in many countries, including the United States. The development and progression of cancer is known to be affected by diet. Modern diets typically include both ω-6 and ω-3 fatty acids, in varying ratios according to culture, geography, food availability, and the like.
Cyclooxygenases (COXs) are membrane-bound enzymes that catalyze conversion of the ω-6 fatty acid arachidonic acid (AA) to metabolites such as prostaglandins and thromboxane. Some prostaglandins, such as prostaglandin-2 (PG2), are known to promote cancer. Research suggests that ω-6 fatty acids may be implicated in cancer due to the formation of deleterious metabolites, such as prostaglandin-2 (PG-2), from cyclooxygenase-2 (COX-2)-catalyzed peroxidation of the ω-6 fatty acid arachidonic acid. Overexpression of COX-2 is often observed in cancer patients, thereby amplifying the damaging effects of cancer in these individuals.
Two forms of COX, COX-1 and COX-2, are known. COX-2 appears to be selectively turned on and is the form commonly overexpressed in cancer cells and tumors, thus overexpression of COX-2 is considered a major problem in cancer cell initiation, growth, and spread. Conventional COX-2 inhibition strategy (COX-2 inhibitors) aiming to limit cancer promoter formation has been intensively investigated as an anti-cancer treatment strategy and/or to complement chemotherapies to treat all types of cancers. However COX-2 is continues to be observed in cancer patients even after inhibitor treatment, thus the strategy of COX-2 inhibition is often ineffective. Additionally, inhibition of COX-2 may result in safety concerns. For example, COX-2 inhibitors used to control COX-2 levels during cancer treatment can severely injure the gastrointestinal tract and increase the risk of cardiovascular disease.